Medial prefrontal cortex lesions abolish contextual control of competing responses

There is much debate as to the extent and nature of functional specialization within the different subregions of the prefrontal cortex. The current study was undertaken to investigate the effect of damage to medial prefrontal cortex subregions in the rat. Rats were trained on two biconditional discrimination tasks, one auditory and one visual, in two different contexts. At test, they received presentations of audiovisual compounds of these training stimuli in extinction. These compounds had dictated either the same (congruent trials) or different (incongruent trials) responses during training. In sham-operated controls, contextual cues came to control responding to conflicting information provided by incongruent stimulus compounds. Experiment 1 demonstrated that this contextual control of responding was not evident in individual rats with large amounts of damage that included the prelimbic and cingulate subregions of the prefrontal cortex. Experiment 2 further dissociated the result of Experiment 1, demonstrating that lesions specific to the anterior cingulate cortex were sufficient to produce a deficit early on during presentation of an incongruent stimulus compound but that performance was unimpaired as presentation progressed. This early deficit suggests a role for the anterior cingulate cortex in the detection of response conflict, and for the medial prefrontal cortex in the contextual control of competing responses, providing evidence for functional specialization within the rat prefrontal cortex.     

Activation of adenosine receptors in the posterior cingulate cortex impairs memory retrieval in the rat

Adenosine A1 and A2A receptor agonists and antagonists have been reported to alter learning and memory. The aim of our study was to investigate the involvement of adenosinergic system in memory retrieval into posterior cingulate cortex (PCC) of Wistar rats. To clarify this question, we tested specifics agonist and antagonists of adenosine A1 and A2A receptors in rats submitted to a one-trial inhibitory avoidance task. The stimulation of adenosine A1 and A2A receptors by CPA and CGS21680, respectively, impaired memory retrieval for inhibitory avoidance task, into PCC. These findings provide behavioral evidence for the role of adenosinergic system in the memory retrieval into PCC.     

Auditory repetition priming is impaired in pure alexic patients

Alexia without agraphia, or "pure" alexia, is an acquired impairment in reading that leaves writing skills intact. Repetition priming for visually presented words is diminished in pure alexia. However, it is not possible to verify whether this priming deficit is modality-specific or modality independent because reading abilities are compromised. Hence, auditory repetition priming was assessed with lexical decision and word stem completion tasks in pure alexic patients with lesions in left inferior temporal-occipital cortex and the splenium. Perceptually based, modality-specific priming models predict intact auditory priming, since auditory association cortex is spared in the patients. Alternatively, modality-independent models, which suggest that priming reflects the temporary modification of an amodal system, might predict impairments. Baseline performance was matched in the patients and controls, although lexical decision priming measures showed an interaction between group and repetition lag. The patients showed intact immediate priming but significantly less priming than controls at longer delays. Furthermore, word stem completion priming was abolished in the patients. One explanation for the deficit is that left inferior temporal-occipital cortex supports amodal aspects of priming, as suggested by recent neuroimaging results. Another possibility is that long-term auditory priming relies on covert orthographic representations which were unavailable in the patients. The results provide support for interactive models of word identification.     

What, if anything, is the medial temporal lobe, and how can the amygdala be part of it if there is no such thing?

Should the medial temporal lobe (MTL) of primates--which includes allocortical structures such as the hippocampus, neocortical structures such as the parahippocampal cortex, and nuclear structures such as the basolateral amygdala--be considered a single "thing"? According to the prevailing view, here termed the reification theory, the answer is yes. According to this theory, the MTL functions as an amalgamated entity that provides the neuronal mechanisms for declarative memory; the greater the damage to the MTL or any of its components, the greater the deleterious effects on declarative memory. A countervailing view, here called the balkanization theory, holds that the various components of the MTL process and store different kinds of information. According to this theory, damage to each part of the MTL causes a unique set of behavioral deficits-some involving memory, others involving perception, and yet others involving response selection. The empirical neuropsychological evidence favors the balkanization theory, as do some new concepts in theoretical neuroanatomy.     

The role of inferior frontal cortex in phonological processing

Recent neuroimaging studies of language processing are examining the neural substrate of phonology because of its critical role in mapping sound information onto higher levels of language processing (e.g., words) as well as providing codes in which verbal information can be temporarily stored in working memory. However, the precise role of the inferior frontal cortex in spoken and written phonological tasks has remained elusive. Although lesion studies have indicated the presence of selective deficits in phonological processing, the location of lesions underlying these impairments has not revealed a consistent pattern. Despite efforts to refine methods and tasks, functional neuroimaging studies have also revealed variability in activation patterns. Reanalysis of evidence from these neuroimaging studies suggests that there are functional subregions within the inferior frontal gyrus that correspond to specific components of phonological processing (e.g., orthographic to phonological conversion in reading, and segmentation in speech).     

Lesions in the Central Nucleus of the Amygdala: Discriminative Avoidance Learning, Discriminative Approach Learning, and Cingulothalamic Training-Induced Neuronal Activity

The amygdala is critically involved in discriminative avoidance learning. Large lesions of the amygdala block discriminative avoidance learning and abolish cingulothalamic training-induced neuronal activity. These results indicated that amygdalar processing is critical for cingulothalamic plasticity. The larger lesions did not allow differentiation of the specific functioning of various amygdalar nuclei. Anatomical analysis showed that damage in the central (CE) nucleus of the amygdala was correlated with the severity of the behavioral deficit. The present study was carried out to determine whether smaller lesions, centered in the CE nucleus, would impair discriminative avoidance learning and block cingulothalamic plasticity. In addition, the possible role of the CE nucleus in appetitively motivated discriminative approach learning was examined for the first time. New Zealand White rabbits with CE nuclear lesions were first trained in the discriminative approach task. After attaining asymptotic performance, discriminative avoidance training sessions were alternated with continuing approach training sessions, one session each day. The rabbits with lesions were severely impaired in avoidance learning but showed no impairment of approach learning. Surprisingly, the attenuating effects of the lesions on cingulothalamic training-induced neuronal activity were more prevalent during approach learning than during avoidance learning. These results indicated that avoidance learning can be impaired by lesions centered in the CE nucleus that leave cingulothalamic plasticity largely intact and that the CE nucleus is involved in extra-cingulothalamic learning processes.     

盲人的跨感觉通道重组

失去视觉的盲人往往伴随着行为代偿,如听觉和触觉能力的提高。脑成像等认知神经科学研究发现,盲人行为代偿的神经机制之一是大脑皮层的跨感觉通道重组,即盲人的视皮层并没有因为视觉剥夺而失去作用,而是广泛地参与了其他感知觉任务。原本暂时的神经联结由于受到新的感觉信息传入方式的持续激活而固化,从而形成新的神经回路,可能是此类跨通道重组的神经基础。     

猜谜作业中顿悟的ERP效应

采用事件相关电位(ERP)探索问题解决过程中顿悟的神经机制。以猜谜作业为实验程序,对“有顿悟”和“无顿悟”答案引发的脑电分别进行叠加和平均,并将二者相减（有顿悟-无顿悟）得到差异波。在250~500 ms “有顿悟”比“无顿悟”的ERP波形有一个更加负性的偏移,在差异波中,这个负成分的潜伏期约为380 ms（N380）。地形图和电流密度图显示,N380在额中央区活动最强。偶极子源定位分析结果显示,N380可能起源于扣带前回。因此,N380可能反映顿悟问题解决过程中思维定势的突破。     

大脑前扣带回皮层与执行功能

回顾了近期有关大脑前扣带回皮层（ACC）参与执行功能的研究资料。结果显示,ACC可以对正在进行的目标定向行为实施在线监控,在出现反应冲突或错误时提供信号,以便能及时调整与分配注意资源,因此可能是一个行为规划与执行的高级调控结构。这两年来的新发现提示,ACC的执行监控作用可能是基于动机与奖赏期待做出的对“意志行动”的整合性控制,并可能具有对行动结果的情绪评价意义。     

On the emergence of modern humans

The emergence of modern humans with their extraordinary cognitive capacities is ascribed to a novel type of cognitive computational process (sustained non-routine multi-level operations) required for abstract projectuality, held to be the common denominator of the cognitive capacities specific to modern humans. A brain operation (latching) that allows this novel computational process is proposed as well as a physics-inspired mechanism that could explain its rather recent emergence without invoking unlikely genetic or structural changes.